title: Towards improved animal models for evaluating social cognition and its disruption in schizophrenia: the CNTRICS initiative.
abstract: Social cognition refers to processes used to monitor and interpret social signals from others, to decipher their state of mind, emotional status and intentions, and select appropriate social behaviour. Social cognition is sophisticated in humans, being embedded with verbal language and enacted in a complex cultural environment. Its disruption characterises the entire course of schizophrenia and is correlated with poor functional outcome. Further, deficits in social cognition are related to impairment in other cognitive domains, positive symptoms (paranoia and delusions) and negative symptoms (social withdrawal and reduced motivation). In light of the significance and inadequate management of social cognition deficits, there is a need for translatable experimental procedures for their study, and identification of effective pharmacotherapy. No single paradigm captures the multi-dimensional nature of social cognition, and procedures for assessing ability to infer mental states are not well-developed for experimental therapeutic settings. Accordingly, a recent CNTRICS meeting prioritised procedures for measuring a specific construct: "acquisition and recognition of affective (emotional) states", coupled to individual recognition. Two complementary paradigms for refinement were identified: social recognition/preference in rodents, and visual tracking of social scenes in non-human primates (NHPs). Social recognition is disrupted in genetic, developmental or pharmacological disease models for schizophrenia, and performance in both procedures is improved by the neuropeptide oxytocin. The present article surveys a broad range of procedures for studying social cognition in rodents and NHPs, discusses advantages and drawbacks, and focuses on development of social recognition/preference and gaze-following paradigms for improved study of social cognition deficits in schizophrenia and their potential treatment.
authors.affiliation: Unit for Research and Discovery in Neuroscience, IDR Servier, 125 Chemin de Ronde, 78290 Croissy-sur-Seine, France. Electronic address: mark.millan@fr.netgrs.com.
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Millan
authors.forename: Karen L
authors.initials: KL
authors.lastname: Bales
mesh_terms: D000818:Animals; D003072:Cognition Disorders / Q000175:diagnosis* / Q000209:etiology*; D004195:Disease Models, Animal; D006801:Humans; D012559:Schizophrenia / Q000150:complications*; D012919:Social Behavior
keywords: Affective behaviour; Antipsychotic; Emotion; Eye-tracking; Gaze; Mouse; Negative symptoms; Non-human primate; Oxytocin; Psychosis; Rat; Sociability; Social recognition